OP0147 COMPARED TO PEOPLE WHO NEVER SMOKED, CURRENT SMOKERS BUT NOT FORMER SMOKERS HAVE WORSE KNEE OSTEOARTHRITIS SYMPTOMS AND STRUCTURAL DEFECTS: INDIVIDUAL PARTICIPANT DATA META-ANALYSES OF MULTI-COHORT DATA
Authors: Z. Salis, A. Sainsbury-Salis
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> As smoking causes inflammation, and inflammation is implicated in the development of osteoarthritis, it is conceivable that smoking would have negative effects on knee osteoarthritis (KOA). However, results from prior studies are controversial and unclear, with some studies even finding that smoking protects against KOA. <h3>Objectives</h3> To describe the association between smoking and KOA (symptoms and structural defects) in people with or at risk of KOA in a multi-cohort study using individual participant data (IPD) meta-analyses, which are considered the 'gold standard' for the synthesis of quantitative evidence. <h3>Methods</h3> We performed IPD meta-analyses using data from three independent cohorts: the Osteoarthritis Initiative (OAI) and the Multicenter Osteoarthritis Study (MOST) from the USA; and the Cohort for Hip and Cohort for Knee (CHECK) from the Netherlands. We assessed the association between smoking status at baseline (never smokers; current smokers; and former smokers) and the outcomes of symptoms and structural defects in KOA, either cross-sectionally at baseline or longitudinally over 4 to 5 years of follow-up. For symptoms, we assessed pain, disability, and stiffness using the Western Ontario and McMaster Universities Arthritis Index (WOMAC). For structural defects, we assessed overall structural defects and three individual structural features (i.e., joint space narrowing; osteophytes on the femoral surface; and osteophytes on the tibial surface), on both the lateral and medial sides of the knee, from radiographs. Overall structural defects were assessed using Kellgren-Lawrence (KL) grades. A knee with a KL grade ≥ 2 is considered to have 'radiographic KOA'. The three individual structural features were assessed using Osteoarthritis Research Society International (OARSI) grades. <h3>Results</h3> We investigated 14,470 knees from 7,304 participants for the outcomes of symptoms, and 12,337 knees from 6,455 participants for the outcomes of structural defects. In our cross-sectional analyses, compared to never smokers, current smokers had baseline scores for pain, disability, and stiffness that were greater by 1.01 (95% confidence interval [CI] 0.60 to 1.41) units, 3.62 (95% CI 2.04 to 5.20) units, and 0.42 (95% CI: 0.29 to 0.54) units, respectively. In contrast, former smokers had baseline scores for pain, disability, and stiffness that were no different from those of never smokers (with differences in scores being 0.11 95% CI: -0.08 to 0.29 units; -0.09 95% CI: -1.14 to 0.97 units; and 0.06 95% CI: -0.08 to 0.20 units, respectively). In terms of structural defects, our cross-sectional analyses showed that neither current smokers nor former smokers were any worse than never smokers with respect to grades for overall structural defects or individual structural features. However, compared to never smokers, current smokers had greater odds of having radiographic KOA (odds ratio [OR] 1.25 95% CI: 1.02 to 1.52), while former smokers were no different from never smokers for this outcome (OR 0.91 95% CI: 0.83 to 1.01). In our longitudinal analyses, compared to never smokers, only one outcome showed a difference between groups. Specifically, current smokers had greater odds of degeneration of the individual structural feature of joint space narrowing on the medial side of the knee over 4 to 5 years of follow-up (OR 1.27 95% CI: 1.01 to 1.60), while former smokers were no different from never smokers for this outcome (OR 1.02 95% CI: 0.84 to 1.24). <h3>Conclusion</h3> Current smoking may have negative effects on, and quitting smoking could be important in preventing or slowing, both the symptoms and structural defects of KOA in people with or at risk of KOA. <h3>Acknowledgements</h3> We acknowledge the contributions of the study participants, investigators, research staff involved, and the provision of data sets and/or research tools from 3 cohort studies: the OAI, the MOST study, and the CHECK study. <h3>Disclosure of Interests</h3> Zubeyir Salis: None declared, Amanda Sainsbury-Salis Speakers bureau: presentation fees and travel reimbursements from Eli Lilly and Co, the Pharmacy Guild of Australia, Novo Nordisk, the Dietitians Association of Australia, Shoalhaven Family Medical Centres, the Pharmaceutical Society of Australia, and Metagenics., Consultant of: Served on the Nestlé Health Science Optifast VLCD advisory board from 2016 to 2018.